Plus Kits ELISA pour Sclerostin partenaires d'interaction

Human Sclerostin (SOST) interaction partners

Sclerostin is degraded by cathepsin K in vitro. Cathepsin K degradation of sclerostin is affected by hypoxia.

Study found that sclerostin concentrations were not significantly higher in patients with bone metastases compared to non-metastatic prostate cancer (PC) but they were significantly higher in patients with CRPC. Sclerostin levels were significantly higher in patients with advanced disease and increased bone turnover due to a compensatory response to the increased number of osteoblasts.

Patients with Latent autoimmune diabetes in Adults (LADA) presented lower bone resorption than did controls, similar to patients with T2 diabetes (T2D). Sclerostin is increased in T2D but not in LADA, suggesting possible roles on bone metabolism in T2D only.

Higher Sclerostin/SOST expression is associated with lower percentage of circulatory blasts and better prognosis in patients with myelofibrosis.

Sclerosteosis is caused by loss-of-function mutations in the SOST gene which encodes a secreted glycoprotein, sclerostin--{REVIEW}

Serum sclerostin level was not an independent predictor of mortality in Maintenance Hemodialysis Patients

these results suggest a possible role of sclerostin in the identification of ankylosing spondylitis patients

important role for SOST SNP rs1877632 and VDR SNPs rs10735810 and rs731236 in the pathophysiology of stress fracture

In our cohort of pregnant women, sclerostin and DKK1 were not associated with any adverse metabolic profile, and possibly do not play relevant roles in the pathophysiology of gestational diabetes mellitus.

serum sclerostin levels correlated positively with carotid intima-media thickness and inversely with the augmentation index, a marker of arterial stiffness

The difference of serum sclerostin levels in Ankylosing Spondylitis and Rheumatoid Arthritis patients was not significantly different from HC, indicating that the sclerostin may not associate with the development of Ankylosing Spondylitis and Rheumatoid Arthritis.

No difference was found in the serum sclerostin levels between the hyperthyroidism patients and healthy control.

Positivity of RANKL and anti-CCP2 yielded significant risk for progression with negativity for both as reference. No single nucleotide polymorphism encoding TNFSF11 or SOST was associated with increased concentrations of the factors.

Osterix and RUNX2 are transcriptional regulators of sclerostin in human bone

Sclerostin But Not Dickkopf-1 has roles in increasing prevalence of osteoporotic fracture and lower bone mineral density in postmenopausal Korean women

An association was found between rs851054 of the SOST promoter and the fracture rate during childhood osteogenesis imperfecta.

High serum levels of sclerostin and Dkk-1 are associated with acute ischaemic stroke

The increased expression of sclerostin in the liver and the association with histologic cholangitis may explain the high serum levels of this protein in patients with primary biliary cirrhosis.

Mouse (Murine) Sclerostin (SOST) interaction partners

Study demonstrated that sclerostin is expressed in chondrocytes and upregulates the early stage of chondrogenic differentiation in vitro. Furthermore, sclerostin downregulates the expression of markers associated with the late stage of chondrogenic differentiation.

The SOST gene inhibited the expression of COL1, OCN, and OPN, reduced the activity of alkaline phosphatase, and increased the expression of LPL and PPARgamma.

Since adipocytes do not produce sclerostin, these findings suggest an unexplored endocrine function for sclerostin that facilitates communication between the skeleton and adipose tissue.

A microtubule-dependent mechanotransduction pathway that linked fluid shear stress to reactive oxygen species and calcium (Ca2+) signals that led to a reduction in sclerostin abundance in cultured osteocytes.

our study provided histological evidences that sclerostin tends to be secreted in osteocytes of remodeled mature bone, while FGF23 would be differently synthesized in osteoblasts and osteocytes according to the developmental stages

These results show that osteocytes and/or osteoblasts secrete factors regulating beige adipogenesis, at least in part, through the Wnt-signaling inhibitor sclerostin.

In vivo muCT analysis of cortical bone at age 1 and 3 months confirmed increased thickness in Sost-/-mice, but revealed no cortical abnormalities in single Gja1+/-or Sost+/-mice

complete absence of sclerostin has only minor effects on chronic kidney disease-induced bone loss in mice.

In mice, sclerostin deficiency hastened reparative dentinogenesis after pulp injury, suggesting that the inhibition of sclerostin may constitute a promising therapeutic strategy for improving the healing of damaged pulps.

These data suggest that sclerostin plays an important role in the bone remodeling of tooth movement.

Analysis of SOST expression using large minigenes reveals the MEF2C binding site in the evolutionarily conserved region (ECR5) enhancer mediates forskolin, but not 1,25-dihydroxyvitamin D3 or TGFbeta1 responsiveness.

removal of sclerostin appears to modestly protect the alveolar bone from resorption in this experimental setting

Sclerostin (SOST) profil antigène

Antigen Summary

Sclerostin is a secreted glycoprotein with a C-terminal cysteine knot-like (CTCK) domain and sequence similarity to the DAN (differential screening-selected gene aberrative in neuroblastoma) family of bone morphogenetic protein (BMP) antagonists. Loss-of-function mutations in this gene are associated with an autosomal-recessive disorder, sclerosteosis, which causes progressive bone overgrowth. A deletion downstream of this gene, which causes reduced sclerostin expression, is associated with a milder form of the disorder called van Buchem disease.